title: Patients treated with interferon-alpha, interferon-beta, and interleukin-2 have a different thyroid autoantibody pattern than patients suffering from endogenous autoimmune thyroid disease.
abstract: Cytokines are believed to mediate the induction and perpetuation of autoimmune thyroid disease (ATD) in humans. However, this concept is mainly based on in vitro findings and to date, concrete in vivo evidence is still lacking. This prompted us to compare serum thyroid parameters of patients treated with cytokines with patients suffering from ATD. The cytokine group (n = 61) consisted of patients suffering from chronic hepatitis (n = 27) and from hemato-oncological diseases (n = 34). Patients were treated with interferon-alpha (IFN-alpha) or IFN-beta, either alone (n = 31) or in combination with interleukin-2 (IL-2) (n = 15) or with antineoplastic agents (n = 15). The ATD group (n = 105) consisted of 51 patients with Graves' disease, 26 with euthyroid ATD, 18 with Hashimoto's disease, and 10 with atrophic thyroiditis. Only 6 of 61 patients (10%) from the cytokine-treated group had thyroid peroxidase antibody (TPOAb) titers equal to or greater than 100 U/mL, whereas 82 of 87 patients (94%) suffering from ATD had TPOAb titers equal to or greater than 100 U/mL (p = 0.0001). In contrast, the percentage of patients who had thyroglobulin antibody (TgAb) serum titers equal to or greater than 100 U/mL were identical in both groups: 25 of 61 patients (41%) treated with cytokines versus 40 of 87 patients (46%) suffering from ATD (p = 0.789). Thus, patients with ATD had significantly higher TPOAb titers (p = 0.0001) whereas TgAb titers were not significantly different compared with patients from the cytokine group. The substantial difference in autoantibody response raises the possibility that thyroid abnormalities associated with ATD reflect genetic susceptibility and/or an independent stimulus or incident aside from cytokine dysfunction and that cytokines may play a secondary, rather than primary role in disease expression.
authors.affiliation: Department of Clinical Endocrinology, Hannover Medical School, FRG.
authors.forename: F
authors.initials: F
authors.lastname: Schuppert
authors.forename: E
authors.initials: E
authors.lastname: Rambusch
authors.forename: H
authors.initials: H
authors.lastname: Kirchner
authors.forename: J
authors.initials: J
authors.lastname: Atzpodien
authors.forename: L D
authors.initials: LD
authors.lastname: Kohn
authors.forename: A
authors.initials: A
authors.lastname: von zur Mühlen
mesh_terms: D000328:Adult; D000368:Aged; D000970:Antineoplastic Agents / Q000009:adverse effects / Q000627:therapeutic use*; D001323:Autoantibodies / Q000097:blood / Q000187:drug effects* / Q000276:immunology*; D016207:Cytokines / Q000009:adverse effects / Q000627:therapeutic use*; D005260:Female; D006801:Humans; D016898:Interferon-alpha / Q000009:adverse effects / Q000627:therapeutic use; D016899:Interferon-beta / Q000009:adverse effects / Q000627:therapeutic use; D007376:Interleukin-2 / Q000009:adverse effects / Q000627:therapeutic use; D007453:Iodide Peroxidase / Q000276:immunology; D008297:Male; D008875:Middle Aged; D013954:Thyroglobulin / Q000276:immunology; D013961:Thyroid Gland / Q000276:immunology* / Q000473:pathology; D013967:Thyroiditis, Autoimmune / Q000139:chemically induced / Q000276:immunology*
chemical_list: D000970:Antineoplastic Agents; D001323:Autoantibodies; D016207:Cytokines; D016898:Interferon-alpha; D007376:Interleukin-2; D016899:Interferon-beta; D013954:Thyroglobulin; D007453:Iodide Peroxidase